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MiR-31 promotes mammary stem cell expansion and breast tumorigenesis by suppressing Wnt signaling antagonists.

文献类型：期刊论文

作者Sheng XL3; Tian YH3; Shuai JW2; Ren FZ3; Cui W3,12; Lengner C1,11,13; Dai X8; Plikus MV9; Xu MG8; Jiao BW7
刊名NATURE COMMUNICATIONS
出版日期2017
卷号8期号:X页码:e1036
英文摘要MicroRNA-mediated post-transcriptional regulation plays key roles in stem cell self-renewal and tumorigenesis. However, the in vivo functions of specific microRNAs in controlling mammary stem cell (MaSC) activity and breast cancer formation remain poorly understood. Here we show that miR-31 is highly expressed in MaSC-enriched mammary basal cell population and in mammary tumors, and is regulated by NF-κB signaling. We demonstrate that miR-31 promotes mammary epithelial proliferation and MaSC expansion at the expense of differentiation in vivo. Loss of miR-31 compromises mammary tumor growth, reduces the number of cancer stem cells, as well as decreases tumor-initiating ability and metastasis to the lung, supporting its pro-oncogenic function. MiR-31 modulates multiple signaling pathways, including Prlr/Stat5, TGFβ and Wnt/β-catenin. Particularly, it activates Wnt/β-catenin signaling by directly targeting Wnt antagonists, including Dkk1. Importantly, Dkk1 overexpression partially rescues miR31-induced mammary defects. Together, these findings identify miR-31 as the key regulator of MaSC activity and breast tumorigenesis.
语种英语
资助机构Z.Y. is supported by the National Natural Science Foundation of China (No. 81572614,31271584); Beijing Nature Foundation Grant (5162018); the Major Project for Cultiva tion Technology (2016ZX08008001, 2014ZX08008001); National Dairy Industry and Technology System (No.CARS-36); Basic Research Program (2015QC0104, 2015TC041, 2016SY001, 2016QC086); SKLB Open Grant (2015SKLB6-16). M.V.P. is supported by the NIH NIAMS grants R01-AR067273, R01-AR069653. J.S. is supported by the National Natural Science Foundation of China (No. 31370830 and 11675134) and the 111 Project (No. B16029). ; Z.Y. is supported by the National Natural Science Foundation of China (No. 81572614,31271584); Beijing Nature Foundation Grant (5162018); the Major Project for Cultiva tion Technology (2016ZX08008001, 2014ZX08008001); National Dairy Industry and Technology System (No.CARS-36); Basic Research Program (2015QC0104, 2015TC041, 2016SY001, 2016QC086); SKLB Open Grant (2015SKLB6-16). M.V.P. is supported by the NIH NIAMS grants R01-AR067273, R01-AR069653. J.S. is supported by the National Natural Science Foundation of China (No. 31370830 and 11675134) and the 111 Project (No. B16029). ; Z.Y. is supported by the National Natural Science Foundation of China (No. 81572614,31271584); Beijing Nature Foundation Grant (5162018); the Major Project for Cultiva tion Technology (2016ZX08008001, 2014ZX08008001); National Dairy Industry and Technology System (No.CARS-36); Basic Research Program (2015QC0104, 2015TC041, 2016SY001, 2016QC086); SKLB Open Grant (2015SKLB6-16). M.V.P. is supported by the NIH NIAMS grants R01-AR067273, R01-AR069653. J.S. is supported by the National Natural Science Foundation of China (No. 31370830 and 11675134) and the 111 Project (No. B16029). ; Z.Y. is supported by the National Natural Science Foundation of China (No. 81572614,31271584); Beijing Nature Foundation Grant (5162018); the Major Project for Cultiva tion Technology (2016ZX08008001, 2014ZX08008001); National Dairy Industry and Technology System (No.CARS-36); Basic Research Program (2015QC0104, 2015TC041, 2016SY001, 2016QC086); SKLB Open Grant (2015SKLB6-16). M.V.P. is supported by the NIH NIAMS grants R01-AR067273, R01-AR069653. J.S. is supported by the National Natural Science Foundation of China (No. 31370830 and 11675134) and the 111 Project (No. B16029).
源URL[http://159.226.149.26:8080/handle/152453/12082]  
专题昆明动物研究所_遗传资源与进化国家重点实验室
昆明动物研究所_发育的印迹调控与进化学
通讯作者zyu@cau.edu.cn
作者单位1.Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
2.Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
3.State Key Laboratories for Agrobiotechnology and Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Biological Sciences, China Agricultural University, Beijing, 100193, China.
4.Department of Biochemistry and Molecular Biology, Hebei Key Laboratory of Chinese Medicine Research on Cardio-Cerebrovascular Disease, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050200, China.
5.Department of Biochemistry and Molecular Biology, Basic Medical College, Tianjin Medical University, Tianjin, 300070, China.
6.Institute of Reproductive and Developmental Biology, Department of Surgery and Cancer, Imperial College London, London, W12 0NN, UK.
7.Department of Physics and State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, Xiamen University, Xiamen, 361005, China
8.Vanderbilt University Medical Center, Nashville, TN, 37232, USA.
9.State Key Laboratory of Genetic Resources and Evolution of Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, 650223, China
10.Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
推荐引用方式
GB/T 7714		 Sheng XL,Tian YH,Shuai JW,et al. MiR-31 promotes mammary stem cell expansion and breast tumorigenesis by suppressing Wnt signaling antagonists.[J]. NATURE COMMUNICATIONS,2017,8(X):e1036.
APA Sheng XL.,Tian YH.,Shuai JW.,Ren FZ.,Cui W.,...&Yu ZY*.(2017).MiR-31 promotes mammary stem cell expansion and breast tumorigenesis by suppressing Wnt signaling antagonists..NATURE COMMUNICATIONS,8(X),e1036.
MLA Sheng XL,et al."MiR-31 promotes mammary stem cell expansion and breast tumorigenesis by suppressing Wnt signaling antagonists.".NATURE COMMUNICATIONS 8.X(2017):e1036.

入库方式： OAI收割

来源：昆明动物研究所

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